Salinity has a significant influence on the physiology of freshwater aquatic organisms. However, there are few studies on the hematology and immunology of freshwater fish under high salinity. In the current study, we aimed to analyze the adaptive effect of salt stress on L. capito spleen immune function and hematology using transcriptomic analysis. We replicated a L. capito acute salinity stress model, and collected blood and spleens from freshwater and saltwater fish. It was found that salinity affected significantly the numbers of leukocytes, lymphocytes, neutrophils, and red blood cells, as well as the content of haemoglobin. Salt treatment resulted in a significant increase in the expression of HSP70, HSP90, CAT, SOD, and GPX1 genes in L. capito spleens. Transcriptomic analysis revealed a total of 546 differentially expressed genes (DEGs) in spleens, including 224 up-regulated DEGs and 322 down-regulated DEGs. In addition, GO enrichment analysis revealed immune system process, multicellular organismal process, and biological regulation of genes with the most differences in biological processes. KEGG enrichment analysis showed that the regulation of lipolysis in adipocyte, FoxO signaling pathway, Hematopoietic cell lineage signaling pathway, and HIF-1 signaling pathway were significantly enriched. L. capito adapted oxidative to high salinity through FoxO signaling pathway and immune to high salinity through Hematopoietic cell lineage signaling pathway. At the same time, we selected 10 DEGs for qRT-PCR detection, and the results showed that the qRT-PCR results were consistent with our RNA-Seq results, indicating that transcriptome sequencing was accurate and reliable. In conclusion, our results demonstrated that the improvement of antioxidant capacity, heat shock protein and immunity are involved in the molecular mechanism of L. capito adapting to high salinity. Our findings provided a rationale for further study on high salinity adaptation and related enrichment pathways.

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http://dx.doi.org/10.1016/j.marpolbul.2023.115017DOI Listing

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